Crosstalk between hydrogen sulfide and nitric oxide in endothelial cells.
Bottom Line: Their interaction at different levels would have a profound impact on angiogenesis.Blockade of NO production by eNOS-specific siRNA or nitro-L-arginine methyl ester (L-NAME) reversed, but eNOS overexpression potentiated, the proliferative effect of H2 S on ECs.Our results suggest that H2 S stimulates the phosphorylation of eNOS through a p38 MAPK and Akt-dependent pathway, thus increasing NO production in ECs and vascular tissues and contributing to H2 S-induced angiogenesis.
Affiliation: Department of Biology, Lakehead University, Thunder Bay, Ontario, Canada.Show MeSH
Mentions: NaHS (50 and 100 μM) treatment markedly increased the phosphorylation of eNOS in ECs (Fig. 2A). The stimulatory effect of NaHS on eNOS phosphorylation was time dependent, and the increase in phosphorylated eNOS appeared at 10 min., peaked at 30 min., and gradually declined to baseline over the period of 1-hr NaHS exposure (Fig. 2B). NaHS treatment up to 36 hrs had no significant effect on eNOS expression level (Fig. 2C).
Affiliation: Department of Biology, Lakehead University, Thunder Bay, Ontario, Canada.